| Literature DB >> 25686534 |
Francisco Westermeier1, Mario Navarro-Marquez1, Camila López-Crisosto1, Roberto Bravo-Sagua1, Clara Quiroga1, Mario Bustamante1, Hugo E Verdejo2, Ricardo Zalaquett2, Mauricio Ibacache3, Valentina Parra4, Pablo F Castro2, Beverly A Rothermel5, Joseph A Hill5, Sergio Lavandero6.
Abstract
Diabetic cardiomyopathy (DCM) is a common consequence of longstanding type 2 diabetes mellitus (T2DM) and encompasses structural, morphological, functional, and metabolic abnormalities in the heart. Myocardial energy metabolism depends on mitochondria, which must generate sufficient ATP to meet the high energy demands of the myocardium. Dysfunctional mitochondria are involved in the pathophysiology of diabetic heart disease. A large body of evidence implicates myocardial insulin resistance in the pathogenesis of DCM. Recent studies show that insulin signaling influences myocardial energy metabolism by impacting cardiomyocyte mitochondrial dynamics and function under physiological conditions. However, comprehensive understanding of molecular mechanisms linking insulin signaling and changes in the architecture of the mitochondrial network in diabetic cardiomyopathy is lacking. This review summarizes our current understanding of how defective insulin signaling impacts cardiac function in diabetic cardiomyopathy and discusses the potential role of mitochondrial dynamics.Entities:
Keywords: Diabetic cardiomyopathy; Insulin signaling; Mitochondrial dynamics
Mesh：
Substances：
Year: 2015 PMID： 25686534 PMCID： PMC4626247 DOI： 10.1016/j.bbamcr.2015.02.005
Source DB: PubMed Journal: Biochim Biophys Acta ISSN： 0006-3002